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Neurocritical Care Aug 2022Following aneurysmal subarachnoid hemorrhage (SAH), patients are monitored closely for vasospasm in the intensive care unit. Conditional vasospasm-free survival...
BACKGROUND
Following aneurysmal subarachnoid hemorrhage (SAH), patients are monitored closely for vasospasm in the intensive care unit. Conditional vasospasm-free survival describes the risk of future vasospasm as a function of time elapsed without vasospasm. Conditional survival has not been applied to this clinical scenario but could improve patient counseling and intensive care unit use. The objective of this study was to characterize conditional vasospasm-free survival following SAH.
METHODS
This was a single institution, retrospective cohort study of patients treated for aneurysmal SAH between 1/1/2000-6/1/2020. The primary outcome was the development of vasospasm defined by the first instance of either radiographic vasospasm on computed tomography angiography, Lindegaard Index > 3.0 by transcranial doppler ultrasonography, or vasospasm-specific intraarterial therapy. Multivariable Cox regression was performed, and conditional vasospasm-free survival curves were constructed.
RESULTS
A total of 528 patients were treated for aneurysmal SAH and 309 (58.5%) developed vasospasm. Conditional survival curves suggest patients who survive to postbleed day 10 without vasospasm have a nearly 90% chance of being discharged without vasospasm. The median onset of vasospasm was postbleed day 6. Age more than 50 years was associated with a lower risk (hazard ratio [HR] = .76; 95% confidence interval [CI] 0.64-0.91; p < 0.001). Higher initial systolic blood pressure (HR = 1.18; 95% CI 1.046-1.350; p = .008), Hunt-Hess grades 4 or 5 (HR = 1.304; 95% CI 1.014-1.676), and modified Fisher scale score of 4 (HR = 1.808; 95% CI 1.198-2.728) were associated with higher vasospasm than the respective lower grades.
CONCLUSION
Conditional survival provides a useful framework for counseling patients and making decisions around vasospasm risk for patients with aneurysmal SAH, while risk factor-stratified plots facilitate a patient-centric, evidence-based approach to these conversations and decisions.
Topics: Autonomic Nervous System Diseases; Humans; Middle Aged; Retrospective Studies; Risk Factors; Subarachnoid Hemorrhage; Ultrasonography, Doppler, Transcranial; Vasospasm, Intracranial
PubMed: 35099712
DOI: 10.1007/s12028-022-01444-z -
Fluids and Barriers of the CNS Nov 2023Cerebral vasospasm significantly contributes to poor prognosis and mortality in patients with aneurysmal subarachnoid hemorrhage. Current research indicates that the... (Review)
Review
Cerebral vasospasm significantly contributes to poor prognosis and mortality in patients with aneurysmal subarachnoid hemorrhage. Current research indicates that the pathological and physiological mechanisms of cerebral vasospasm may be attributed to the exposure of blood vessels to toxic substances, such as oxyhaemoglobin and inflammation factors. These factors disrupt cerebral vascular homeostasis. Vascular homeostasis is maintained by the extracellular matrix (ECM) and related cell surface receptors, such as integrins, characterised by collagen deposition, collagen crosslinking, and elastin degradation within the vascular ECM. It involves interactions between the ECM and smooth muscle cells as well as endothelial cells. Its biological activities are particularly crucial in the context of cerebral vasospasm. Therefore, regulating ECM homeostasis may represent a novel therapeutic target for cerebral vasospasm. This review explores the potential pathogenic mechanisms of cerebral vasospasm and the impacts of ECM protein metabolism on the vascular wall during ECM remodelling. Additionally, we underscore the significance of an ECM protein imbalance, which can lead to increased ECM stiffness and activation of the YAP pathway, resulting in vascular remodelling. Lastly, we discuss future research directions.
Topics: Humans; Vasospasm, Intracranial; Endothelial Cells; Extracellular Matrix; Subarachnoid Hemorrhage; Extracellular Matrix Proteins; Collagen
PubMed: 37925414
DOI: 10.1186/s12987-023-00483-8 -
Neurological Research and Practice 2019Aneurysmatic Subarachnoid Haemorrhage (aSAH) is typically caused by extravasated blood in the subarachnoid space due to a ruptured aneurysm. aSAH is often...
INTRODUCTION
Aneurysmatic Subarachnoid Haemorrhage (aSAH) is typically caused by extravasated blood in the subarachnoid space due to a ruptured aneurysm. aSAH is often life-threatening in the acute stage, but may also cause secondary brain damage due to delayed cerebral ischaemia (DCI) and other complications in the days and weeks after the initial bleeding. Rapid onset of a most severe headache is a typical sign of a non-traumatic aSAH besides a reduced level of consciousness and neurologic deficits.
FIRST STEPS
Immediate diagnostic steps in case of a suspected SAH are cerebral imaging (CCT, MRI) and lumbar puncture. If a SAH is confirmed, a digital subtraction angiography should be performed to detect an aneurysm. If an aneurysm is detected it should be occluded immediately after interdisciplinary consultation with neurosurgeons and neuroradiologists.
COMMENTS
If endovascular coiling and surgical clipping are both available and equally suitable, coiling should be preferred due to a better long-time outcome. Often the age of the patient, the location of the aneurysm, and the configuration of the aneurysm result in favouring one or the other technique. Special care aims at avoiding stress, increased intracranial pressure, pain, fever, emesis, and at keeping glucose levels and electrolytes in the normal range. As nimodipine is associated with a better outcome, it should be administered from the beginning. To detect vasospasm, serial transcranial doppler should be performed at least once a day for at least 14 days. If vasospasms are detected, this procedure needs to be continued until flow velocity returns to the normal range. To detect an increased intracranial pressure, external ventricular drainage or intraparenchymal probes are recommended. Regarding haemodynamics, euvolaemia and normotension should be achieved. If vasospasms and/or an increased intracranial pressure occur, mean arterial pressure needs to be adjusted to ensure an adequate cerebral perfusion pressure.
CONCLUSIONS
If immediate actions are taken to treat the aneurysm and complications in the following weeks are handled with care, a favourable outcome is possible for this otherwise often devastating disease.
PubMed: 33324881
DOI: 10.1186/s42466-019-0015-3 -
Neurology India 2019This article highlights the pathogenesis and management of cerebral vasospasm. It discusses the various pharmacological, endovascular, and neurosurgical approaches... (Review)
Review
This article highlights the pathogenesis and management of cerebral vasospasm. It discusses the various pharmacological, endovascular, and neurosurgical approaches available for the treatment of cerebral vasospasm. Numerous drugs and procedures have been tried and tested in the management of cerebral vasospasm. We try to highlight the pros and cons of various pharmacological agents and case-based use of other not so popular and investigational techniques.
Topics: Brain Ischemia; Humans; Subarachnoid Hemorrhage; Vasospasm, Intracranial
PubMed: 30860121
DOI: 10.4103/0028-3886.253627 -
BioMed Research International 2014Subarachnoid hemorrhage (SAH) can lead to devastating neurological outcomes, and there are few pharmacologic treatments available for treating this condition. Both... (Review)
Review
Subarachnoid hemorrhage (SAH) can lead to devastating neurological outcomes, and there are few pharmacologic treatments available for treating this condition. Both animal and human studies provide evidence of inflammation being a driving force behind the pathology of SAH, leading to both direct brain injury and vasospasm, which in turn leads to ischemic brain injury. Several inflammatory mediators that are elevated after SAH have been studied in detail. While there is promising data indicating that blocking these factors might benefit patients after SAH, there has been little success in clinical trials. One of the key factors that complicates clinical trials of SAH is the variability of the initial injury and subsequent inflammatory response. It is likely that both genetic and environmental factors contribute to the variability of patients' post-SAH inflammatory response and that this confounds trials of anti-inflammatory therapies. Additionally, systemic inflammation from other conditions that affect patients with SAH could contribute to brain injury and vasospasm after SAH. Continuing work on biomarkers of inflammation after SAH may lead to development of patient-specific anti-inflammatory therapies to improve outcome after SAH.
Topics: Biomarkers; Brain Injuries; Humans; Inflammation; Inflammation Mediators; Subarachnoid Hemorrhage; Vasospasm, Intracranial
PubMed: 25105123
DOI: 10.1155/2014/384342 -
CNS Neuroscience & Therapeutics Oct 2019Aneurysmal subarachnoid hemorrhage (aSAH) continues to be associated with significant morbidity and mortality despite advances in care and aneurysm treatment strategies.... (Review)
Review
Aneurysmal subarachnoid hemorrhage (aSAH) continues to be associated with significant morbidity and mortality despite advances in care and aneurysm treatment strategies. Cerebral vasospasm continues to be a major source of clinical worsening in patients. We intended to review the clinical and experimental aspects of aSAH and identify strategies that are being evaluated for the treatment of vasospasm. A literature review on aSAH and cerebral vasospasm was performed. Available treatments for aSAH continue to expand as research continues to identify new therapeutic targets. Oral nimodipine is the primary medication used in practice given its neuroprotective properties. Transluminal balloon angioplasty is widely utilized in patients with symptomatic vasospasm and ischemia. Prophylactic "triple-H" therapy, clazosentan, and intraarterial papaverine have fallen out of practice. Trials have not shown strong evidence supporting magnesium or statins. Other calcium channel blockers, milrinone, tirilazad, fasudil, cilostazol, albumin, eicosapentaenoic acid, erythropoietin, corticosteroids, minocycline, deferoxamine, intrathecal thrombolytics, need to be further investigated. Many of the current experimental drugs may have significant roles in the treatment algorithm, and further clinical trials are needed. There is growing evidence supporting that early brain injury in aSAH may lead to significant morbidity and mortality, and this needs to be explored further.
Topics: Calcium Channel Blockers; Endovascular Procedures; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Subarachnoid Hemorrhage; Vasodilator Agents; Vasospasm, Intracranial
PubMed: 31583833
DOI: 10.1111/cns.13222 -
Current Neurovascular Research 2021The correlation of neuroinflammation with the development of cerebral vasospasm following subarachnoid hemorrhage has been well documented in the literature; both... (Review)
Review
The correlation of neuroinflammation with the development of cerebral vasospasm following subarachnoid hemorrhage has been well documented in the literature; both clinical and preclinical. The exact mechanisms by which this process occurs, however, are poorly elucidated. Recent evidence indicates that interleukin-6 is not only an important prognostic biomarker for subarachnoid hemorrhage and subsequent vasospasm development but also an integral component in the progression of injury following initial insult. In this review, we briefly highlight other pathways under investigation and focus heavily on what has been discovered regarding the role of interleukin 6 and cerebral vasospasm following subarachnoid hemorrhage. A proposed mechanistic pathway is highlighted in written and graphical format. A discussion regarding the human correlative findings and initial pre-clinical mechanistic studies is addressed. Finally, in the future investigation section, innovative developments and a clear description of areas warranting further scientific inquiry are emphasized. This review will catalyze continued discovery in this area of emerging significance and aid in the quest for effective vasospasm treatment where limited clinical therapeutics currently exist.
Topics: Humans; Interleukin-6; Subarachnoid Hemorrhage; Vasospasm, Intracranial
PubMed: 34736380
DOI: 10.2174/1567202618666211104122408 -
Neurocritical Care Aug 2021Cerebral vasospasm is a major contributor to disability and mortality after aneurysmal subarachnoid hemorrhage. Oxidation of cell-free hemoglobin plays an integral role...
BACKGROUND
Cerebral vasospasm is a major contributor to disability and mortality after aneurysmal subarachnoid hemorrhage. Oxidation of cell-free hemoglobin plays an integral role in neuroinflammation and is a suggested source of tissue injury after aneurysm rupture. This study sought to determine whether patients with subarachnoid hemorrhage and cerebral vasospasm were more likely to have been exposed to early hyperoxemia than those without vasospasm.
METHODS
This single-center retrospective cohort study included adult patients presenting with aneurysmal subarachnoid hemorrhage to Vanderbilt University Medical Center between January 2007 and December 2017. Patients with an ICD-9/10 diagnosis of aneurysmal subarachnoid hemorrhage were initially identified (N = 441) and subsequently excluded if they did not have intracranial imaging, arterial PaO values or died within 96 h post-rupture (N = 96). The final cohort was 345 subjects. The degree of hyperoxemia was defined by the highest PaO measured within 72 h after aneurysmal rupture. The primary outcome was development of cerebral vasospasm, which included asymptomatic vasospasm and delayed cerebral ischemia (DCI). Secondary outcomes were mortality and modified Rankin Scale.
RESULTS
Three hundred and forty five patients met inclusion criteria; 218 patients (63%) developed vasospasm. Of those that developed vasospasm, 85 were diagnosed with delayed cerebral ischemia (DCI, 39%). The average patient age of the cohort was 55 ± 13 years, and 68% were female. Ninety percent presented with Fisher grade 3 or 4 hemorrhage (N = 310), while 42% presented as Hunt-Hess grade 4 or 5 (N = 146). In univariable analysis, patients exposed to higher levels of PaO by quintile of exposure had a higher mortality rate and were more likely to develop vasospasm in a dose-dependent fashion (P = 0.015 and P = 0.019, respectively). There were no statistically significant predictors that differentiated asymptomatic vasospasm from DCI and no significant difference in maximum PaO between these two groups. In multivariable analysis, early hyperoxemia was independently associated with vasospasm (OR = 1.15 per 50 mmHg increase in PaO2 [1.03, 1.28]; P = 0.013), but not mortality (OR = 1.10 [0.97, 1.25]; P = 0.147) following subarachnoid hemorrhage.
CONCLUSIONS
Hyperoxemia within 72 h post-aneurysmal rupture is an independent predictor of cerebral vasospasm, but not mortality in subarachnoid hemorrhage. Hyperoxemia is a variable that can be readily controlled by adjusting the delivered FiO and may represent a modifiable risk factor for vasospasm.
Topics: Adult; Aneurysm, Ruptured; Brain Ischemia; Female; Humans; Infant, Newborn; Retrospective Studies; Subarachnoid Hemorrhage; Vasospasm, Intracranial
PubMed: 33150573
DOI: 10.1007/s12028-020-01136-6 -
Diagnostic and Interventional Imaging 2015Complications of subarachnoid hemorrhage are the major life threatening and functional components of the follow up of a ruptured aneurysm. Knowing how to identify these... (Review)
Review
Complications of subarachnoid hemorrhage are the major life threatening and functional components of the follow up of a ruptured aneurysm. Knowing how to identify these is a key challenge. They vary in type throughout the postoperative follow up period. The aim of this article is firstly to list the main complications of the acute phase (rebleeding, acute hydrocephalus, acute ischemic injury and non-neurological complications), the subacute phase (vasospasm) and the chronic phase of subarachnoid hemorrhages: (chronic hydrocephalus and cognitive disorders) and to describe their major clinical and radiological features. Secondly, we describe the long-term follow up strategy for patients who have suffered a subarachnoid hemorrhage and have been treated endovascularly or by surgery. This follow up involves a combination of clinical consultations, cerebral MRI and at least one review angiogram.
Topics: Aneurysm, Ruptured; Brain Damage, Chronic; Brain Ischemia; Cerebral Angiography; Cognition Disorders; Embolization, Therapeutic; Follow-Up Studies; Humans; Hydrocephalus; Image Processing, Computer-Assisted; Magnetic Resonance Imaging; Recurrence; Subarachnoid Hemorrhage; Surgical Instruments; Tomography, X-Ray Computed; Vasospasm, Intracranial
PubMed: 26119863
DOI: 10.1016/j.diii.2015.05.006 -
RoFo : Fortschritte Auf Dem Gebiete Der... Jan 2018
Topics: Adult; Cerebral Angiography; Computed Tomography Angiography; Diagnosis, Differential; Headache Disorders, Primary; Humans; Magnetic Resonance Imaging; Male; Nimodipine; Subarachnoid Hemorrhage; Syndrome; Vasoconstriction; Vasospasm, Intracranial
PubMed: 28950385
DOI: 10.1055/s-0043-119891